ArticleNucleic acids research2013
Cell cycle stage-specific roles of Rad18 in tolerance and repair of oxidative DNA damage.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Neuronal Injury and Regeneration-Linked Gene Expression Dynamics in the Hypothalamic-Pituitary-Adrenal Axis Following Experimental Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026Review
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisNAR cancer · 2026Article
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisbioRxiv : the preprint server for biology · 2025Article
- Ubiquitination of the histone variant mH2A1.2 prevents toxic RAD18 accumulation at a subset of genomic loci upon replication stress.Molecular cell · 2025Article
- Detection of endogenous translesion DNA synthesis in single mammalian cells.Cell reports methods · 2023Article
- Genome-wide CRISPR screen identified Rad18 as a determinant of doxorubicin sensitivity in osteosarcoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Timely termination of repair DNA synthesis by ATAD5 is important in oxidative DNA damage-induced single-strand break repair.Nucleic acids research · 2021Article
- Adverse outcome pathways for ionizing radiation and breast cancer involve direct and indirect DNA damage, oxidative stress, inflammation, genomic instability, and interaction with hormonal regulation of the breast.Archives of toxicology · 2020Review
- Replication protein A dynamically regulates monoubiquitination of proliferating cell nuclear antigen.The Journal of biological chemistry · 2019Article
- Pyruvate kinase M2 regulates homologous recombination-mediated DNA double-strand break repair.Cell research · 2018Article
- The Cancer/Testes (CT) Antigen HORMAD1 promotes Homologous Recombinational DNA Repair and Radioresistance in Lung adenocarcinoma cells.Scientific reports · 2018Article
- Selective human inhibitors of ATR and ATM render Leishmania major promastigotes sensitive to oxidative damage.PloS one · 2018Article
- Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis.Cell cycle (Georgetown, Tex.) · 2018Review
- DNA repair factor RAD18 and DNA polymerase Polκ confer tolerance of oncogenic DNA replication stress.The Journal of cell biology · 2017Article
- Mechanisms of Post-Replication DNA Repair.Genes · 2017Review
- Forging Ahead through Darkness: PCNA, Still the Principal Conductor at the Replication Fork.Molecular cell · 2017Review
- Oxidative stress at low levels can induce clustered DNA lesions leading to NHEJ mediated mutations.Oncotarget · 2016Article
- Tumor suppressor miR-145 reverses drug resistance by directly targeting DNA damage-related gene RAD18 in colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The E3 ubiquitin ligase Rad18 mediates tolerance of replication fork-stalling bulky DNA lesions, but whether Rad18 mediates tolerance of bulky DNA lesions acquired outside S-phase is unclear. Using synchronized cultures of primary human cells, we defined cell cycle stage-specific contributions of Rad18 to genome maintenance in response to ultraviolet C (UVC) and H(2)O(2)-induced DNA damage. UVC and H(2)O(2) treatments both induced Rad18-mediated proliferating cell nuclear antigen mono-ubiquitination during G(0), G(1) and S-phase. Rad18 was important for repressing H(2)O(2)-induced (but not ultraviolet-induced) double strand break (DSB) accumulation and ATM S1981 phosphorylation only during G(1), indicating a specific role for Rad18 in processing of oxidative DNA lesions outside S-phase. However, H(2)O(2)-induced DSB formation in Rad18-depleted G1 cells was not associated with increased genotoxin sensitivity, indicating that back-up DSB repair mechanisms compensate for Rad18 deficiency. Indeed, in DNA LigIV-deficient cells Rad18-depletion conferred H(2)O(2)-sensitivity, demonstrating functional redundancy between Rad18 and non-homologous end joining for tolerance of oxidative DNA damage acquired during G(1). In contrast with G(1)-synchronized cultures, S-phase cells were H(2)O(2)-sensitive following Rad18-depletion. We conclude that although Rad18 pathway activation by oxidative lesions is not restricted to S-phase, Rad18-mediated trans-lesion synthesis by Polη is dispensable for damage-tolerance in G(1) (because of back-up non-homologous end joining-mediated DSB repair), yet Rad18 is necessary for damage tolerance during S-phase.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.